Pigment gallstones are a common cause of biliary tract disease in Americans and account for about 1/3 of the half-million cholecystectomies performed yearly. From our data it is clear that patients in the general population have pigment gallstones, and from other studies that patients with hemolysis and/or cirrhosis have a high incidence of pigment gallstones. Yet, the etiology of pigment stone disease is unknown. Human studies of bile obtained at cholecystectomy or by duodenal drainage may be of limited value since changes in bile may reflect the presence of stones or cholecystitis. Furthermore prospective studies in man would require decades of observation. Thus, an animal model of human pigment stones is ideal. We are utilizing the laboratory mouse (nb/nb) with a hereditary hemolytic anemia and spontaneously formed pigment gallstones as a model of human pigment lithiasis. Our objectives are to characterize this mouse model and to determine pathogenesis, prevention and/or treatment of pigment stones in these mice. Thereby, the data obtained will be applied to better understand human pigment lithiasis.